Lachenmeier Dirk W, Kanteres Fotis, Rehm Jürgen
Chemisches und Veterinäruntersuchungsamt (CVUA) Karlsruhe, Karlsruhe, Germany.
Addiction. 2009 Apr;104(4):533-50. doi: 10.1111/j.1360-0443.2009.02516.x.
In addition to being produced in ethanol metabolism, acetaldehyde occurs naturally in alcoholic beverages. Limited epidemiological evidence points to acetaldehyde as an independent risk factor for cancer during alcohol consumption, in addition to the effects of ethanol. This study aims to estimate human exposure to acetaldehyde from alcoholic beverages and provide a quantitative risk assessment.
The human dietary intake of acetaldehyde via alcoholic beverages was estimated based on World Health Organization (WHO) consumption data and literature on the acetaldehyde contents of different beverage groups (beer, wine, spirits and unrecorded alcohol). The risk assessment was conducted using the European Food Safety Authority's margin of exposure (MOE) approach with benchmark doses obtained from dose-response modelling of animal experiments. Life-time cancer risk was calculated using the T25 dose descriptor.
The average exposure to acetaldehyde from alcoholic beverages was estimated at 0.112 mg/kg body weight/day. The MOE was calculated to be 498, and the life-time cancer risk at 7.6 in 10,000. Higher risk may exist for people exposed to high acetaldehyde contaminations, as we have found in certain unrecorded alcohol beverages in Guatemala and Russia, for which we have demonstrated possible exposure scenarios, with risks in the range of 1 in 1000.
The life-time cancer risks for acetaldehyde from alcoholic beverages greatly exceed the usual limits for cancer risks from the environment set between 1 : 10,000 and 1 : 1,000,000. Alcohol consumption has thus been identified as a direct source of acetaldehyde exposure, which in conjunction with other sources (food flavourings, tobacco) results in a magnitude of risk requiring intervention. An initial public health measure could be to reduce the acetaldehyde content in alcoholic beverages as low as technologically possible, and to restrict its use as a food flavour additive.
乙醛除了在乙醇代谢过程中产生外，还天然存在于酒精饮料中。有限的流行病学证据表明，除乙醇的影响外，乙醛是饮酒期间癌症的独立危险因素。本研究旨在估计人类从酒精饮料中接触乙醛的情况，并提供定量风险评估。
根据世界卫生组织（WHO）的消费数据以及不同饮料组（啤酒、葡萄酒、烈酒和未记录酒精饮料）中乙醛含量的文献，估算人类通过酒精饮料摄入乙醛的情况。使用欧洲食品安全局的暴露边际（MOE）方法进行风险评估，该方法采用从动物实验剂量反应模型获得的基准剂量。使用T25剂量描述符计算终生癌症风险。
估计从酒精饮料中平均接触乙醛的量为0.112毫克/千克体重/天。计算得出的MOE为498，终生癌症风险为万分之7.6。对于接触高乙醛污染的人群，可能存在更高的风险，正如我们在危地马拉和俄罗斯的某些未记录酒精饮料中发现的那样，我们已经展示了可能的接触情况，风险范围为千分之一。
酒精饮料中乙醛导致的终生癌症风险大大超过通常设定的环境癌症风险限值（万分之一至百万分之一）。因此，饮酒已被确定为乙醛暴露的直接来源，这与其他来源（食品调味剂、烟草）一起导致了需要干预的风险程度。初步的公共卫生措施可以是在技术上尽可能降低酒精饮料中的乙醛含量，并限制其作为食品调味添加剂的使用。
